IgA nephropathy (IgAN) is the most common form of glomerulonephritis (GN) worldwide. The onset of IgAN may be associated with an upper respiratory tract infection [1,2]. Frequently, C3 and other classes of immunoglobulin deposits are detected in a pattern similar to the IgA. The most common histopathologic alterations include focal or diffuse expansion of mesangial regions with proliferative cells and extracellular matrix [3]. Additionally, a wide variety of lesions may be seen in patients with more severe lesions, including diffuse endocapillary proliferation, segmental sclerosis, segmental necrosis, and cellular crescent formation [4,5]. And reactive oxygen species (ROS) have been reported to play a major pathogenic role in the development of a wide range of human and experimental glomerular disorders, including IgAN [6-8]. Although IgAN is considered an immune complex disease resulting from IgA-immune complex (IgA-IC) glomerular damage, the cause of the disease and the pathogenic mechanisms that propagate this disease are unknown.
Although glucocorticoid steroids have been used to treat some of IgAN patients, their efficacy in preserving the deterioration of renal function in IgAN remains largely unclear, and the long-term use of these drugs can cause severe adverse side effects because of potential uncontrollable immunosuppressive effects [9-11].
Ginsenosides, the main active ingredients of ginseng, are known to have a variety of pharmacological activities, e.g. antitumor, antidiabetic, antifatique, antiallergic and antioxidant activities. Ginsenosides share a basic structure, composed of gonane steroid nucleus having 17 carbon atoms arranged in four rings. Ginsenosides are metalized in the body, and a number of recent studies suggest that ginsenoside metabolites, rather than naturally occurring ginsenosides, are readily absorbed in the body and act as the active components. Among them, ginsenoside M1 is known as one metabolite of protopanaxadiol-type ginsenosides via the gypenoside pathway by human gut bacteria. Until now, no prior art references report the effect of ginsenoside M1 in treatment of IgAN.